In a cooperative agreement starting January 1995, prior to the FDA’s licensure of the varicella vaccine on March 17, the Centers for Disease Control and Prevention (CDC) funded the Los Angeles Department of Health Services’ Antelope Valley Varicella Active Surveillance Project (AV-VASP). Since only varicella case reports were gathered, baseline incidence data for herpes zoster (HZ) or shingles was lacking.

VLA COMMENT: The near eradication of the early childhood Chicken Pox has resulted in people who have had natural wild chickenpox as children are not getting their”subtle” exongenous boosters from the subsequent generation of our children or our grandchildren who unfortunately are prevented from getting wild chicken pox, They are getting vaccinated with a different strain that can’t boost us. So, in essence, the CDC has simply brought another chicken pox strain into existence. Now we have two. However, the wild typeis not prevelant enough to give us the necessary booster so we don’t get shingles.

Dr. Gary Goldman: The reason why we are getting SHINGLES

The only reason that “children who get the chickenpox vaccine APPEAR to have a much lower risk of shingles” is that the live vaccine has provided these children with a recent boost to their immunity. However, the vaccine-strain of varicella zoster virus (VZV)–also known as the Oka strain–is genetically different from the wild-type U.S. strain. When a vaccinated child is exposed to an adult with shingles or a child with wild-type varicella, if the strains are sufficiently heterologous, the vaccinated child will break out in chickenpox. It is also possible for the weakened vaccine-strain to revert to a more virulent strain that manifests wild-type pathology. This means when children are exposed to the wild-type strain, even though they may not have a breakthrough infection with chickenpox, they now harbor two heterologous (genetically different) strains of VZV–both of which are at a later time subject to reactivation as shingles. Thus, as they age, they will be even more likely to reactivate with shingles (unless periodically administered booster vaccine doses for life in order to maintain the immunity)–especially if they do not receive exogenous (outside) boosts to their cell-mediated immunity which, in the pre-vaccine era, came from expostures to other children infected with wild-type varicella which provided the adult with a subclinical boost that helped to suppress or postpone reactivattion of shingles.

I would also like to clear up the point that shingles has always been increasing–even prior to the licensing of the varicella vaccine. This statement is true; however, the increases were on the order of 2 to 4% per year (which were likely due to an aging population, or greater access to healthcare). Once a community had widespread distribution of varicella vaccine, increases in herpes zoster were on the order of 20% per year. For example, this source [Yih WK, Brooks DR, Lett SM, et al. The incidence of varicella and herpes zoster in Massachusetts as measured by the Behavioral Risk Factor Surveillance System (BRFSS) during a period of increasing varicella vaccine coverage, 1998-2003. BMC Public Health 2005; 5:68.
32. Schmid DS, Jumaan AO. Impact of varicella vaccine on varicella-zoster virus dynamics. Clin Microbiol Rev 2010; 23(1):202–217] found a 90% increase in shingles over 5 years (1999-2003).